健胃愈疡颗粒对胃溃疡大鼠胃组织MK、和表皮生长因子受体表达的影响

目的：探讨健胃愈疡颗粒的疗效及抗复发机制。方法：以Okabe改良法复制大鼠实验性胃溃疡,采用免疫组织化学和原位杂交技术,观察该药对胃溃疡组织Midkine(MK)和表皮生长因子受体（EGFR）表达的影响。结果：模型组MK和EGFR的表达较正常组增高,而健胃愈疡治疗组MK和EGFR的表达增高较模型组更为明显。结论：健胃愈疡颗粒可增加MK和EGFR的上增性表达,这可能是其促进溃疡愈合和提高溃疡愈合质量从而减少溃疡复发的物质基础。     

乙酸性胃溃疡大鼠一氧化氮、内皮素及表皮生长因子受体相互关系研究

目的 :探讨一氧化氮 (NO)、内皮素 (ET- 1)、表皮生长因子受体 (EGFR)在乙酸性慢性胃溃疡大鼠中的作用及相互关系。方法 :采用乙酸性慢性胃溃疡疾病模型 ,游标卡尺测定溃疡指数 ,硝酸还原酶法测定 NO含量 ,放射免疫法检测血浆 ET- 1含量 ,SABC免疫组织化学方法及图像分析观察 EGFR在溃疡周围粘膜的表达。结果 :左旋精氨酸 (L - Arg)组溃疡指数与模型组及亚硝基左旋精氨酸 (L - NNA )组比较显差有显著性意义 (P <0 .0 5 ,<0 .0 1) ;L- Arg组血清 NO及血浆 ET- 1含量与对照组、模型组及 L- NNA组比较差异有显著性意义 (P <0 .0 5 ,<0 .0 1) ;L - NNA组血清 NO及血浆 ET- 1含量与模型组及对照组比较差异均有非常显著性意义 (均 P <0 .0 1) ;L -Arg组 EGFR表达较模型组、L- NNA组及对照组显著增加 (积分光密度值及阳性细胞占总面积百分比均 P <0 .0 5 ) ;L- NNA组 EGFR显著弱于模型组 (P<0 .0 1)。结论 :NO前体 L- Arg可以诱导、促进 NO合成 ,反馈性地抑制 ET- 1的释放 ,从而维持 NO和 ET的动态平衡及胃粘膜 EGFR正常水平表达 ,促进溃疡愈合。     

消溃灵对乙酸性胃溃疡大鼠一氧化氮和内皮素的影响

目的：探讨消费灵对消化性溃疡愈合的影响及其胃粘膜保护作用的机制,方法：采用大鼠乙酸性胃溃疡模型,分别以消溃灵灌胃和左旋精氨酸＊（L－Arg),亚硝基左旋精氨酸（L－NNA）腹腔内注射治疗7d 和 14d后,测定溃疡指数,溃疡抑制率,检测血清一氧化氮（NO）及血浆内皮素（ET－1）含量,结果：消溃灵组溃疡指数,血浆ET－1含量明显 降低,而溃疡抑制率,血清NO含量显著升高,与模型组和L＿NNA组比较差异有显著性意义（P＜0．01）,与L－Arg组比较无统计学意义（P＜0．05）,L－NNA组溃疡指数,血浆ET－1水平显著高于模型组（P＜0．01）,而血清NO含量则明显低于模型组（P＜0．01）,结论：消溃灵促进溃疡愈合,保护胃粘膜的作用可能与其诱导,促进NO合成,反馈性地抑制ET－1释放,维持NO和ET的动态平衡密切相关。     

健脾益气中药对乙酸慢性胃溃疡大鼠热休克蛋白表达的影响

目的：研究健脾益气中药对大鼠乙酸慢性胃溃疡修复过程中热休克蛋白（ＨＳＰｓ）的影响,探索ＨＳＰｓ对胃溃疡的病理生理意义。方法：以ＳＡＢＣ免疫组织化学方法观察乙酸慢性胃溃疡大鼠模型溃疡周围胃粘膜的ＨＳＰ７０并进行图像分析,用Ｗｅｓｔｅｒｎ 斑点印迹法检测各组动物血清及胃粘膜匀浆ＨＳＰ２７,６０,７０ 的含量。结果：模型组和雷尼替丁组血清及胃粘膜ＨＳＰ２７,６０,７０ 表达较对照组增加（Ｐ＜ ０．０５,＜ ０．０１）,中药组进一步升高（Ｐ＜ ０．０５,＜ ０．０１）。结论：ＨＳＰ２７,６０,７０可能参与胃溃疡的病理生理过程,健脾益气中药通过ＨＳＰｓ的机制促进溃疡的愈合     

健中愈疡片对乙酸诱导胃溃疡大鼠表皮生长因子及其受体表达的影响

[目的]观察健中愈疡片对乙酸诱导胃溃疡大鼠血清表皮生长因子（EGF）水平和胃溃疡边缘表皮生长因子受体（EGFR）表达的影响。[方法]制备乙酸诱导大鼠胃溃疡模型，分别予健中愈疡片、雷尼替丁和0．85％氯化钠液治疗14d，用放射免疫分析法测定大鼠血清EGF水平，免疫组织化学染色法检测胃溃疡边缘EGFR表达。[结果]造模3d时，胃溃疡模型组大鼠的血清EGF水平明显高于正常对照组，胃溃疡边缘EGFR表达比正常对照组明显增加。治疗14d后，与雷尼替丁组和0．85％氯化钠液组比较，健中愈疡片组的血清EGF水平显著减少（P〈0．01），而胃溃疡边缘EGFR表达显著增加（P〈0．01）。[结论]血清EGF水平可以作为反映胃肠黏膜完整性的一个监控指标，健中愈疡片能够减少血清EGF水平和增加胃溃疡边缘EGFR表达，这可能是其加速乙酸诱导胃溃疡愈合的主要作用机制。     

健脾益气方促进胃黏膜修复机制研究

[目的]研究健脾益气中药对大鼠胃黏膜保护和修复的机制,观察大鼠胃黏膜表皮生长因子受体(EG-FR)和血清一氧化氮(NO)的变化.[方法]采用乙酸致溃疡大鼠模型,以SABC免疫组织化学方法观察溃疡周围胃黏膜的EGFR并进行图像分析,用镀铜镉还原比色法测定血清NO3-/NO2-代表血清NO水平.[结果]模型组胃黏膜EGFR表达较对照组增加(P＜0.01),中药组进一步升高(P＜0.01).模型组血清NO3-/NO2-明显低于对照组(P＜0.01),中药组血清NO3-/NO2-则显著高于模型组(P＜0.01).[结论]中药健脾益气方通过EGFR和NO促进胃粘膜保护和修复.     

胃炎饮对胃溃疡大鼠血清内皮素-1和一氧化氮含量的影响

目的探讨胃炎饮对胃溃疡模型大鼠血清内皮素1(ET-1)、一氧化氮(NO)含量的影响。方法采用冰醋酸腐蚀法建立实验性胃溃疡大鼠模型,以奥美拉唑为对照,观察胃炎饮对实验性胃溃疡大鼠胃粘膜溃疡面积和血清ET-1、NO含量的影响。结果与假手术组相比,模型组的血清ET-1含量明显升高,NO含量明显降低(P0.01);与模型组相比,各用药组溃疡面积均明显缩小(P0.01或P0.05),血清ET-1含量明显下降(P0.01),胃炎饮高、低剂量组的血清NO含量明显升高(P0.01或P0.05)。结论胃炎饮可调节血管舒缩因子,改善胃黏膜循环,从而促进溃疡愈合。     

消溃灵对乙酸性胃溃疡大鼠一氧化氮 和内皮素的影响

探讨消溃灵对消化性溃疡愈合的影响及其胃粘膜保护作用的机制。方法采用大鼠乙酸性胃溃疡模型,分别以消溃灵灌胃和左旋精氨酸(L-Arg)、亚硝基左旋精氨酸(L-NNA)腹腔内注射治疗7d和14d后,测定溃疡指数、溃疡抑制率,检测血清一氧化氮(NO)及血浆内皮素(ET-1)含量。结果消溃灵组溃疡指数、血浆ET-1含量明显降低,而溃疡抑制率、血清NO含量显著升高,与模型组和L-NNA组比较差异有显著性意义(P＜0.01),与L-Arg组比较无统计学意义(P＞0.05)。L-NNA组溃疡指数、血浆ET-1水平显著高于模型组(P＜0.01),而血清NO含量则明显低于模型组(P＜0.01)。结论消溃灵促进溃疡愈合,保护胃粘膜的作用可能与其诱导、促进NO合成,反馈性地抑制ET-1释放,维持NO和ET的动态平衡密切相关。     

猴头菌提取物颗粒治疗胃溃疡临床疗效观察及其作用机制研究

目的观察猴头菌提取物颗粒对胃溃疡患者的临床疗效，并探讨药物的疗效机制。方法将我院收治的胃溃疡患者166例随机分为对照组和治疗组，其中，对照组82例，仅给予常规治疗；治疗组84例，在常规治疗的基础上加服猴头菌提取物颗粒。同时测定治疗前后血清中NO、NOS的改变及胃黏膜中EGF及EGFR的变化。结果治疗组溃疡愈合和胃痛改善症状的总有效率分别为92．9％和97．6％，均明显优于对照组（P〈0．05）；治疗组患者NO、NOS、EGF及EGFR指标较治疗前及对照组均有明显增加。结论猴头菌提取物颗粒治疗胃溃疡临床疗效佳，这可能与其提高NO、NOS、EGF及EGFR水平，促进溃疡愈合有关。     

愈疡1号颗粒对胃溃疡大鼠自由基代谢相关因素的影响

[目的]探讨愈疡1号颗粒对胃溃疡（Gu）大鼠自由基代谢相关因素表达的影响。[方法]应用冰乙酸注射法建立大鼠GU模型,随机分为5组,即正常组、模型组、奥美拉唑组及愈疡1号颗粒高、低剂量（高、低剂量）组,给予相应干预后测定各组大鼠胃黏膜丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH—Px）、一氧化氮（N0）的表达及血清NO水平。[结果]模型组大鼠胃黏膜MDA、NO水平均较正常组显著升高,SOD、GSH—Px活性均较正常组显著降低。与模型组比较,高、低剂量组均能够明显提高大鼠胃黏膜SOD、GSH—Px活性,明显降低MDA、NO水平。高剂量组能明显降低血清NO水平。[结论]愈疡1号颗粒通过降低胃黏膜MDA、NO表达及血清NO水平,提高胃黏膜SOD和GSH-Px的表达,起到保护胃黏膜的作用,是其治疗GU的重要机制之一。     

端粒酶在胃癌及癌前病变组织中的表达及其意义

目的：通过检测胃癌及癌前病变组织端粒酶的活性,探讨在这些病变演化中端粒酶活性表达的规律及其意义。方法：采用端粒酶TRAP－ELISA法定量检测33例胃癌、8例胃粘膜重度异型增生、5例轻度异型增生、 胃粘膜肠上皮化生、19例慢性浅表性胃炎组织端粒酶活性。结果：由慢性浅表性胃炎→胃粘膜肠上皮化生→轻度异型增生→重度异型增生→胃癌,端粒酶阳性率逐渐增高,分别为0％、42．9％、40．0％、75．0％、84．0％。端粒酶阳性率在胃癌及重度异型增生组明显高于其它各组（P＜0．005）。慢性浅表性胃炎与肠上皮化生及轻度异型增生组比较也有显著差异（P＜0．025）,而胃癌与重度异型增生组比较差异无显著性。结论：端粒酶在胃癌的发生中可能具有重要意义。追踪端粒酶阳性的胃癌前病变患者有利于早期发现胃癌。     

Gastric Epithelial Dysplasia in Relapsing and Nonrelapsing Gastric Ulcer

In 50 patients with benign gastric ulcer (eight relapsing, 42 nonrelapsiing) the evolution of the edge and scar histological characteristics was studied with special regard to the pressure and modification of epithelial dysplasia. The patients were endoscopically followed-up for 1 to 74 months. Dysplasia was present in 29% of observations made in active ulcer and in 19% of patients with scarring gastric ulcer. Severe dysplasia was found only in one case. During follow-up, regression of the dysplastic changes was documented in 64% of the cases, progression from mild to moderate dysplasia in 4%, while no change was recorded in 32%. Appearance of dysplasia or progression from mild to moderate was seen in 62% of the relapsing cases, as opposed to 14% of the nonrelapsing cases (p < 0.005). Dysplastic changes, usually mild, are relatively frequent in the mucosa both at the edge and scar of gastric ulcer, but they tend to disappear with the healing of the ulcer. Appearance or progression in severity of dysplasia during follow-up are rare, but significantly more frequent in relapsing ulcers, which therefore require more careful follow-up.     

β-连环蛋白在胃腺瘤和胃癌中的表达及其意义

β-连环蛋白（eatenin）是Wnt信号转导途径异常激活的关键环节，多种肿瘤的发生、发展与B．连环蛋白异常表达密切相关。目的：观察β-连环蛋白在正常胃黏膜、胃腺瘤和胃癌组织中的表达，探讨其在胃癌发生、发展中的作用。方法：取得经胃镜活检病理检查证实的78例不同胃组织标本，包括24例正常胃黏膜、24例胃腺瘤性息肉（胃腺瘤，14例为低级别上皮内瘤变，10例为高级别上皮内瘤变）和30例胃腺癌组织，以免疫组化ABC法检测标本中β-连环蛋白的表达。结果：β-连环蛋白在正常胃黏膜和低级别上皮内瘤变胃腺瘤组织中为细胞膜表达，在高级别上皮内瘤变胃腺瘤和胃腺癌组织中呈细胞质／细胞核异位表达。胃腺癌组织中β-连环蛋白的异常表达率显著高于胃腺瘤组织（100％对41．7％，P〈0．05），膜表达缺失者占76．7％（23／30）。结论：β-连环蛋白异常表达与胃癌的发生、发展密切相关，可能是胃癌发生的早期事件。     

糖尿病大鼠胃排空功能与胃组织瘦素的关系

大量文献已证实瘦素可抑制胃排空，胃排空延迟是糖尿病常见的并发症。目的：探讨不同病期糖尿病胃排空延迟与胃组织瘦素的关系。方法：40只Wistar大鼠分为对照1周组（NC1组）、对照4周组（NC2组）、糖尿病病期1周组（DM1组）和糖尿病病期4周组（DM2组）。分别于注射链佐霉素或柠檬酸缓冲液1、4周后检测大鼠胃排空、胃组织瘦素和瘦索受体OB—RbmRNA的表达。结果：与NC1组相比，DM1组大鼠胃排空明显加快（P〈0．01），胃组织瘦素表达显著增加（P〈0．01），OB—RbmRNA的表达无显著差异。与NC2组相比，DM2组大鼠胃排空明显减缓（P〈0．01），瘦素表达显著降低（P〈0．01），OB—RbmRNA的表达无显著差异。结论：随着糖尿病病期的持续，大鼠胃排空由加速转为延迟．胃组织瘦素表达反馈性由增加转为减少。     

Effect of Somatostatin on Pentagastrin-Stimulated Gastric Acid Secretion and Gastric Antral Motility in Dogs with Gastric Fistula

The purpose of the present study was to evaluate the effect of somatostatin on gastric acid secretion and gastric antral motility in conscious dogs with gastric fistula. Infusion of pentagastrin induced motility with a digestive pattern. Somatostatin inhibited dose-dependently the stimulated acid secretion, whereas the effect on antral motility was more complex, acting especially on the amplitude of the contractions. The effects of somatostatin were not altered by using α-and β-adrenergic, dopaminergic, and serotonergic blocking drugs. The dose-response kinetics with seven doses of pentagastrin with and without somatostatin showed inhibition of a competitive type for gastric acid secretion and of a non-competitive type for antral motility with regard to amplitude.     

Effect of Somatostatin on Bethanechol-Stimulated Gastric Acid Secretion and Gastric Antral Motility in Dogs with Gastric Fistula

Abstract

Objective. Sofosbuvir and simeprevir in combination with standard therapy are now available for the treatment of patients chronically infected with hepatitis C virus (HCV) genotype 1. With boceprevir and telaprevir, four treatment options are, therefore, now available to clinicians. Phase 3 studies conducted with simeprevir and sofosbuvir compared sustained virological response (SVR) data with those obtained with standard combination therapy and did not include a control arm. It is important to quantify the contribution of these molecules compared to the first direct antiviral agents available. Material and methods. For HCV genotype 1 patients, we performed a literature review and compared all SVR data from phase 3 randomized placebo-controlled trials conducted with these four molecules according to virological characteristics (genotype, viral load) and patient characteristics (IL28B polymorphism, stage of fibrosis). Results. Simeprevir and sofosbuvir provide a net gain in terms of SVR compared to boceprevir and telaprevir except in the case of telaprevir for treatment-naïve HCV genotype 1b patients. Sofosbuvir achieves higher SVR rates than simeprevir except for treatment-naïve IL28B CC patients and naïve HCV genotype 1b patient. Further, simeprevir moderately improve SVR rates compared to telaprevir in treatment-naïve patients with F3–F4 fibrosis and with HCV genotype 1a infection. Conclusion. Sofosbuvir and simeprevir greatly improve the virological response rate compared to first-generation protease inhibitors. All of these data may help in guiding the physician’s treatment decisions, based on financial constraints and patient characteristics. These data can be easily updated with future treatment and demonstrate the contribution of new treatment regimens to achieve optimal SVR rates.     

Lysolecithin and Glyceroglucolipids in Gastric Secretion of Patients with Gastric and Duodenal Ulcer

Basal and pentagastrin-stimulated gastric secretions, collected (at 15-min intervals for 1 h) from six duodenal ulcer and six gastric ulcer patients, were analyzed for their content of lecithin, lysolecithin, and glyceroglucolipids. Whereas the glycero-glucolipid concentrations and the molar ratios of lysolecithin to lecithin (2.5:1) in basal and stimulated secretions from patients with duodenal and gastric ulcer were similar, significant (p < 0.01) differences were noted between these two groups with regard to the lysolecithin contents. The basal secretions of patients with duodenal ulcer contained about 4.5-fold less (204 μmol/l) of lysolecithin than those from patients with gastric ulcer (932 μmol/l). After pentagastrin stimulation, the lysolecithin concentrations in the secretion from duodenal ulcer patients rose slightly (to 212 μmol/l), whereas a twofold decrease (to 440 μmol/l) in lysolecithin was observed in the secretion from patients with gastric ulcer. Statistically significant correlation between concentrations of lysolecithin and glyceroglucolipids was only observed in basal (r = 0.85, p < 0.05) and stimulated (r = 0.93, p < 0.01) secretions from patients with gastric ulcer. It is concluded that high concentrations of lysolecithin in the secretion of gastric ulcer patients results in the weakening of the gastric mucosal barrier by depleting its glyceroglucolipid component.     

Comparison of Gastric Electrical Activity and Gastric Emptying in Healthy and Dyspeptic Children

To assess and compare gastric electrical activity and gastric emptying recorded from dyspeptic and healthy children, cutaneous electrogastrography and ultrasound examination of the gastric emptying were simultaneously performed in 52 children with nonulcer dyspepsia and 114 healthy children. Symptoms were scored from 0 (none) to 6 (severe). A higher percentage of tachygastria, a higher instability of gastric power, and a lower post/preprandial ratio were present in dyspeptic children than healthy children. As regards the ultrasound parameters, the fasting antral area and T1/2 were similar in dyspeptic children and controls. Only 32% of dyspeptic children had a normal gastric emptying time vs 66% of healthy children. Marked postprandial antral dilatation was found in the dyspeptic children, which correlated with the total symptom score. Electrogastrographic and gastric emptying parameters show specific differences in dyspeptic children with respect to controls, both fasting and after a meal. The postprandial antral distension correlates with the severity of the symptoms.     

胃癌及癌前病变中p53蛋白的检测及意义

探讨p53蛋白表达与胃癌及癌病变的相互关系,方法：用免疫组化染色示检测33例肠化,26例异型增生和26例胃癌组织中p53蛋白的表达。结果：p53蛋白在胃癌组织中表达率最高（61．5％）,在异型增生和肠化组织中的表达率分别为34．6％和12．1％,组间有显著差异,各期胃癌组织中p53蛋白的表达无显著差异,结论：p53蛋白在胃癌前病变中已有阳性表达,在肠化、异型增生及胃癌组织中,其表达率依次增高,p53蛋白积累主要发生在癌前病变晚期及胃癌早期,其表达与胃癌发生密切相关。